AI Article Synopsis
- Aging affects both our internal body clock and memory capabilities, but the exact relationship between circadian disruptions and memory impairment in older adults is still unclear.
- Researchers found that HDAC3, a protein that represses certain genes, limits long-term memory and synaptic plasticity in the aging hippocampus, while not disrupting regular circadian rhythms.
- They concluded that the gene Per1 is crucial for forming long-term memories and proposed that it's the expression of circadian genes in the hippocampus, rather than changes to the overall circadian clock, that influences memory formation as we age.
Article Abstract
Aging is accompanied by impairments in both circadian rhythmicity and long-term memory. Although it is clear that memory performance is affected by circadian cycling, it is unknown whether age-related disruption of the circadian clock causes impaired hippocampal memory. Here, we show that the repressive histone deacetylase HDAC3 restricts long-term memory, synaptic plasticity, and experience-induced expression of the circadian gene Per1 in the aging hippocampus without affecting rhythmic circadian activity patterns. We also demonstrate that hippocampal Per1 is critical for long-term memory formation. Together, our data challenge the traditional idea that alterations in the core circadian clock drive circadian-related changes in memory formation and instead argue for a more autonomous role for circadian clock gene function in hippocampal cells to gate the likelihood of long-term memory formation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6102273 | PMC |
| http://dx.doi.org/10.1038/s41467-018-05868-0 | DOI Listing |
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